Such ideas are consistent with the documented phenotypes related to ER‐stress in cell lines lacking UFM1 pathway components or in phenotypic observations of UFM1‐linked morbidities that are plausibly ER‐stress driven (e.g. cardiomyopathy, defective haematopoiesis and skeletal dysplasia) [47, 58, 59, 60, 61, 62]. This evidence concerns the gene UFM1 and skeletal dysplasia.